Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha.

Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Research Abstract Details 

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Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Abstract Text:

Alexander Niessner,Kayoko Sato,Elliot L Chaikof,Ines Colmegna, Goronzy,Cornelia M Weyand,

BACKGROUND: Unstable atherosclerotic plaque is characterized by an infiltrate of inflammatory cells. Both macrophages and T cells have been implicated in mediating the tissue injury leading to plaque rupture; however, signals regulating their activation remain unidentified. Infectious episodes have been suspected to render plaques vulnerable to rupture. We therefore explored whether plasmacytoid dendritic cells (pDCs) that specialize in sensing bacterial and viral products can regulate effector functions of plaque-residing T cells and thus connect host infection and plaque instability. METHODS AND RESULTS: pDCs were identified in 53% of carotid atheromas (n=30) in which they localized to the shoulder region and produced the potent immunoregulatory cytokine interferon (INF)-alpha. IFN-alpha transcript concentrations in atheroma tissues correlated strongly with plaque instability (P<0.0001). Plaque-residing pDCs responded to pathogen-derived motifs, CpG-containing oligodeoxynucleotides binding to toll-like receptor 9, with enhanced IFN-alpha transcription (P=0.03) and secretion (P=0.007). IFN-alpha emerged as a potent regulator of T-cell function, even in the absence of antigen recognition. Specifically, IFN-alpha induced a 10-fold increase of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on the surface of CD4 T cells (P<0.0001) and enabled them to effectively kill vascular smooth muscle cells (P=0.0003). CONCLUSIONS: pDCs in atherosclerotic plaque sense microbial motifs and amplify cytolytic T-cell functions, thus providing a link between host-infectious episodes and acute immune-mediated complications of atherosclerosis.

Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Publishing Authors By Initials

A Niessner,K Sato,EL Chaikof,I Colmegna,JJ Goronzy,CM Weyand,

For similar proteins: dna-binding proteins: toll-like receptor 9 research abstracts see: proteins: dna-binding proteins: toll-like receptor 9 research

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Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Circulation

VOLUME: 114

Page Numbers: 2482-9

Journal Abbreviation: Circulation

ISSN: 1524-4539

DAY: 20

MONTH: 11

YEAR: 2006

Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Information

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LANGUAGE: eng

NlmUniqueID: 147763

Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Keywords Mesh Terms:

KEYWORDS: Toll-Like Receptor 9

MESH TERMS: metabolism

Chemical & Substance for Abstract: Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha. Information

Substance Name: Toll-Like Receptor 9

Registry Number: 0

Grant and Affiliation Information for Pathogen-sensing plasmacytoid dendritic cells stimulate cytotoxic T-cell function in the atherosclerotic plaque through interferon-alpha.

AFFILIATION: Kathleen B. and Mason I. Lowance Center for Human Immunology, Emory University School of Medicine, 101 Woodruff Circle, Atlanta, GA 30322, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL 63919

ACRONYM: HL

MEDLINETA: Circulation

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